Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2019 Dec 17;10:2913. doi: 10.3389/fimmu.2019.02913

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

Copyright © 2019 Doz-Deblauwe, Carreras, Arbues, Remot, Epardaud, Malaga, Mayau, Prandi, Astarie-Dequeker, Guilhot, Demangel and Winter.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

PMC Copyright notice

CR3 triggers the Syk/calcineurin/NFATc pathway upon engagement by PGL-I-producing mycobacteria to rewire the innate response. rBCG::PGL-I targets the lectin domain of CR3 on the surface of DCs, PMNs, and MPs. Dectin-1 and CR3 cooperate to induce highly efficient entry of the bacilli. This triggers Syk for translocation of NFATc to the nucleus and initiates a transcriptional program to generate an NF-κB-independent mediator signature. This preferentially PGL-I-triggered pathway does not depend on MYD88 even though both cooperate to induce maximum levels of these mediators.